The protein Dynein‑related protein 1 (Drp1) plays a crucial role in regulating the process of mitochondrial fission, which is known to be associated with the onset and progression of various human diseases. However, the specific impact of Drp1 on bladder cancer has yet to be fully understood. In previous studies, evidence to support the theory that the deubiquitinating enzyme proteasome non‑ATPase regulatory subunit 14 (PSMD14) is responsible for stabilizing and promoting the activity of Drp1, ultimately resulting in increased mitochondrial fission, has been presented. The levels of PSMD14 in both bladder cancer tissues and cells were elevated, as confirmed through immunohistochemical and immunofluorescent staining. Co‑immunoprecipitation and reciprocal co‑IP tests demonstrated that PSMD14 and Drp1 interacted with each other. Upon knockdown of PSMD14, there was a corresponding decrease in Drp1 expression and subsequent inhibition of mitochondrial fission. However, when the Drp1 agonist Mdivi‑1 was applied to cells where PSMD14 expression had been knocked down, a significant increase in cell growth was observed, partially restoring the cancer‑promoting effects of PSMD14 on cell proliferation. In conclusion, these findings suggest that PSMD14 may stimulate bladder cancer cell proliferation by promoting mitochondrial fission through the stabilization of Drp1.

中文翻译：

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去泛素化酶 PSMD14 对 Drp1 的调节和线粒体分裂的增强促进了膀胱癌细胞的增殖。

动力蛋白相关蛋白 1 (Drp1) 在调节线粒体裂变过程中发挥着至关重要的作用，已知线粒体裂变与多种人类疾病的发生和进展有关。然而，Drp1对膀胱癌的具体影响尚未完全了解。在之前的研究中，已经提出了支持这一理论的证据，即去泛素化酶蛋白酶体非 ATP 酶调节亚基 14 (PSMD14) 负责稳定和促进 Drp1 的活性，最终导致线粒体裂变增加。通过免疫组织化学和免疫荧光染色证实，膀胱癌组织和细胞中的 PSMD14 水平均升高。免疫共沉淀和相互共免疫沉淀测试表明 PSMD14 和 Drp1 相互作用。PSMD14 敲低后，Drp1 表达相应减少，随后线粒体裂变受到抑制。然而，当将 Drp1 激动剂 Mdivi-1 应用于 PSMD14 表达被敲低的细胞时，观察到细胞生长显着增加，部分恢复了 PSMD14 对细胞增殖的促癌作用。总之，这些发现表明 PSMD14 可能通过稳定 Drp1 促进线粒体裂变来刺激膀胱癌细胞增殖。